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补体激活对血小板聚集的影响

丁忠仁, 黄守坚, 孙家钧   

  1. 中山医科大学药理教研室, 广州 510089
  • 收稿日期:1997-09-15 修回日期:1997-12-03 出版日期:1998-03-15 发布日期:1998-03-15

Effect of Complement Activation on Platelet Aggregation

Zhong-Ren Ding, Shou-Jian Huang, Jia-Jun Sun   

  1. Department of Pharmacology, Sun Yat-Sen University of Medical Sciences, Guangzhou 510089
  • Received:1997-09-15 Revised:1997-12-03 Online:1998-03-15 Published:1998-03-15

摘要: 本文用电脑控制的血小板聚集仪研究了来源于中华眼镜蛇的眼镜蛇毒因子(CVF)对多种动物与人的富血小板血浆(PRP)及大鼠凝胶过滤的血小板悬液(GFP)的诱导血小板聚集活性。CVF(195 nmol·L-1)引起大鼠PRP的血小板明显变形继之以缓慢的血小板聚集, 仅能引起豚鼠、家兔、狗和人PRP的血小板变形, 但不引起聚集。CVF(195 nmol·L-1)不引起大鼠GFP的血小板聚集, 但可被新鲜血浆恢复, 而经56 ˚C 30分钟处理血浆则无此作用。CVF诱导的大鼠血小板聚集依赖于细胞外Ca2+而不受吲哚美辛(100 mmol·L-1)影响。Ni2+(3 mmol·L-1)和河豚毒素(40 mmol·L-1)分别抑制CVF引起的血小板聚集曲线最大斜率和聚集率。本实验提示CVF能诱导大鼠血小板聚集, 此作用依赖于补体和细胞外Ca2+, 并与Ca2+Na+内流有关, 而与血栓烷(TXA2)通路无关。

关键词: 眼镜蛇毒因子, 血小板聚集, 补体,

Abstract: Objective: To observe that cobra venom factor (CVF) isolated from the venom of Naja naja atra induces platelet aggregation in platelet rich plasma (PRP) and gel-filtered platelet suspension (GFP). Methods: In vitro platelet aggregation in PRP and GFP was quantified turbidimetrically with computer-controlled aggregometer. Results: CVF 195 nmol·L-1 induced a slow aggregation following an obvious metamorphosis of platelets in rat PRP but not in GFP and in other species. CVF-induced rat platelet aggregation depended on extracellular Ca2+ and complements, and was not affected by indomethacin 100 mmol·L-1. Ni2+ 3 mmol·L-1 attenuated the maximal velocity of aggregation (S) without influence on the maximal extent of aggregation (A) of CVF-induced rat platelet aggregation while tetrodotoxin 40 mmol·L-1 attenuated A without influence on S. Conclusion: CVF, a complement activator, elicits slow rat platelet aggregation following an obvious metamorphosis, which depends on Ca2+ and Na+ influx, complements and is unrelated to thromboxane (TXA2) pathway.

Key words: Cobra venom factor, Platelet aggregation, Complements, Calcium ion

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